Biology of Depressive Disorders. Part A: A Systems by William Z. Potter, Fred Grossman (auth.), J. John Mann M.D.,

By William Z. Potter, Fred Grossman (auth.), J. John Mann M.D., David J. Kupfer M.D. (eds.)

This quantity is the 3rd in a chain on depressive disorder. the 1st quantity, entitled Phenomenology of Depressive disease, is dedicated to a de­ scription of depressive disease from a number of views that come with these of the sufferer, the clinician, and the psychiatric researcher. It de­ scribes the foremost subtypes of depressive disorder and locations them within the context of the existence cycle. the second one quantity during this sequence is entitled types of Depres­ sive problems: mental, organic, and Genetic views. This quantity describes a number of significant versions of depressive issues, in­ cluding genetic, cognitive, interpersonal, intrapsychic, and neurobio­ logical versions. The 3rd and fourth volumes take care of the biology of affective problems intimately. those volumes are unusual by way of a triaxial ap­ proach. In quantity III the biology of affective issues is defined from the point of view of person transmitter platforms and neurophysi­ ologic and biologic methods. In quantity IV the biology of melancholy is addressed from the vantage element of symptom elements of de­ pression, and similarities and changes within the biology of melancholy are defined in comparison to different psychiatric problems with clinically overlapping positive aspects comparable to nervousness issues or consuming problems. the consequences on biology of comorbid stipulations similar to nervousness, own­ ity problems, alcoholism, and consuming problems are reviewed. those ap­ proaches include problems with nation as opposed to trait.

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Blunted prolactin responses to these central serotonergic probes have been reported in patients with major depression (Heninger, Charney, & Sternberg, 1984; Meltzer, Perline, Tricou, Lowy, & Robertson, 1984; Siever, Uhde, Jimerson, Lake, Siberman, Post, & Murphy, 1984). There is evidence of an increased cortisol response to 5-hydroxyhyptophan (5-HTP) (Meltzer, Nash, & Ohmori, 1987) that appears to correlate with a history of suicide attempts, and has been suggested as being due to an increase in receptor number, based on findings in the brain of suicide victims.

II. Suicide. Psychiat Res 1980; 3: 225-236. Agren H, Reibring L, Hartvig P, Tedroff J, Bjurling P, Hornfeldt K, Andersson Y, Lundqvist H, Langstrom B: Low brain uptake of L-[ 11 C]5-hydroxytryptophan in major depression: A positron emission tomography study on patients and health volunteers. Acta Psychiat Scand 1991; 83: 449-455. Asberg M: Neurotransmitter monoamine metabolites in the cerebrospinal fluid as risk factors for suicidal behavior. S. Health & Human Services, 1989,2-193-2-212. Asberg M, Bertilsson L, Martensson B, Scalia Tomba GP, Thoren P, TriiskmanBendz L: CSF monoamine metabolites in melancholia.

Garcia-Sevilla JA, Garcia-Vallejo P, Guimon J: Enhanced Clz-adrenoceptor-mediated platelet aggregation in patients with major depressive disorder. Eur J Pharmacol1983; 94: 359-360. Garcia-Sevilla JA, Guimon J, Garcia-Vallejo P, Fuster MJ: Biochemical and functional evidence of supersensitive platelet a 2-adrenoreceptors in major affective disorder: Effect of long-term carbonate treatment. Arch Gen Psychiat 1986; 43: 51-57. Garcia-Sevilla JA, Hollingsworth PJ, Smith CB: Alphaz-adrenoceptors on human platelets: Selective labelling by [3H] clonidine and [3H]yohimbine and competitive inhibition by antidepressant drugs.

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